Cardiovascular disease accounts for nearly fifty percent of deaths in both the developed world and in developing countries. Indeed, the risk of dying from heart disease is greater than the risk from AIDS and all forms of cancer combined. Cardiovascular disease causes 12 million deaths in the world each year. It is the leading cause of death in the U.S., killing some 950,000 people each year. It also accounts for a significant amount of disability and diminished quality of life. Some 60 million people in the U.S. alone have some form of heart disease. Therefore, a great need exists for the advancement of devices and procedures to cure, treat, and correct a wide variety of forms of heart disease.
Normal heart function primarily relies upon the proper function of each of the four valves of the heart, which pass blood through the four chambers of the heart. The four chambers of the heart include the right atrium and left atrium, the upper chambers, and the right ventricle and left ventricle, the lower chambers. The four valves, controlling blood flow in the chambers, include the tricuspid, mitral, pulmonary, and aortic valves. Heart valves are complex structures that rely on the interaction of many components to open and close the valve. More particularly, each of the four valves of the heart have leaflets, comprised of fibrous tissue, which attach to the walls of the heart and aid in controlling the flow of blood through the valve. The mitral valve has two leaflets and the tricuspid valve has three leaflets. The aortic and pulmonary valves have three leaflets that are more aptly termed “cusps,” stemming from their half moon shape.
The cardiac cycle involves the pumping and distribution of both oxygenated and deoxygenated blood within the four chambers. In systole, or the rhythmic contraction of the heart cycle, blood that has been oxygenated by the lungs enters the heart into the left atrium. During diastole, or the resting phase of heart cycle, the left atrial pressure exceeds the left ventricle pressure; thus, oxygenated blood flows through the mitral valve, a one way inflow valve, into the left ventricle. The contraction of the left ventricle in systole pumps the oxygenated blood through the aortic valve, into the aorta, and is passed to the body. When the left ventricle contracts in systole, the mitral valve closes and the oxygenated blood passes into the aorta rather than back through the mitral valve. On the other side of the heart, deoxygenated blood returns from the body and enters the heart through the right atrium. This deoxygenated blood flows through the tricuspid valve into the right ventricle. When the right ventricle contracts, the tricuspid valve closes and the deoxygenated blood is pumped through the pulmonary valve. Deoxygenated blood is directed to the pulmonary vascular bed for oxygenation, and the cardiac cycle repeats itself.
The performance of the cardiac cycle by the various components of the heart is a complex and intricate process. Deficiency in one of the components of the heart or deficiency in the performance of the cardiac cycle most often leads to one or more of the numerous different types of heart disease. One prevalent heart disease condition is aortic valve regurgitation. Aortic valve regurgitation has many levels of severity. Aortic regurgitation is the diastolic flow of blood from the aorta into the left ventricle. Regurgitation is due to incompetence of the aortic valve or disturbance of the valvular apparatus (e.g., leaflets, annulus of the aorta) resulting in diastolic flow of blood into the left ventricular chamber. Incompetent closure of the aortic valve can result from intrinsic disease of the cusp, diseases of the aorta, or trauma. Aortic regurgitation may be a chronic disease process or it may occur acutely, presenting as heart failure. Diastolic reflux through the aortic valve can lead to left ventricular volume overload.
FIG. 1 provides an illustration of a normal aortic valve 101. The perspective of the aortic valve 101 shown in FIG. 1 provides a diagram of a dissected and flattened aortic valve 101 to best illustrate its components. The aortic valve 101 has three cusps or leaflets, the left coronary cusp 105, the right coronary cusp 110, and the non-coronary cusp 115. These three cusps control the flow of blood from the left ventricle into the aorta, which ultimately conveys oxygenated blood to the tissues of the body for their nutrition. Located just above the three cusps, 105, 110, and 115, are the sinuses of the valsalva 125 and each sinus corresponds to each individual cusp. The origins of the coronary arteries are proximate the sinuses of the valsalva 125. As shown in FIG. 1, the orifice 130 for the right coronary artery is located just above the right coronary leaflet cusp 110. Similarly, the orifice 135 for the left coronary artery is located just above the left coronary leaflet cusp 105. Additionally, the aortic valve 101 is juxtaposed with the anterior mitral annulus 120.
In a normal aortic valve 101, when the left ventricle contracts in systole, the aortic valve cusps, 105, 110, and 115, open into the aorta and blood flows from the left ventricle into the aorta. When the left ventricle rests in diastole, the cusps, 105, 110, and 115, meet and close, covering the area of the valve annulus. Therefore, the cusps, 105, 110, and 115, prevent regurgitation, or backflow of blood, into the left ventricle during diastole.
The aortic valve 101 is located in the aortic root of the aorta. The aortic root has two main components, the inner (aorto-ventricular junction) and the outer (sino-tubular junction), which are considered the functional aortic annulus. It is this aortic annulus that supports the fibrous structures of the cusps, 105, 110, and 115.
As shown in FIG. 1, the function of the aortic valve, involves the complex interaction of numerous components. If one of the components or functions of the complicated interaction fails, then aortic valve regurgitation can result. For example, a bicuspid valve, calcification of the cusps, or stenosis or restricted motion of the cusps can lead to aortic regurgitation. Prolonged and/or severe aortic valve regurgitation can lead to compensatory left ventricle dilation. Aortic valve regurgitation is a progressive condition that, if not corrected, can be fatal.
In addition to aortic regurgitation, pulmonic regurgitation is highly prevalent heart disease that causes or contributes to increasing numbers of heart disease each year. Like aortic regurgitation, pulmonic regurgitation involves the incompetence of the pulmonic valve and its failure to completely close. In a normal pulmonic valve, the right ventricle contracts in systole and pumps blood through the open pulmonic valve into the pulmonary artery. Contrastingly, when the right ventricle rests in diastole, the pulmonic valve closes and prevents the backflow of blood into the right ventricle. In cases of pulmonic regurgitation, the pulmonic valve fails to completely close and permits a regurgitant flow of blood from the pulmonary artery back into the right ventricle during diastole. This backflow of blood can overload the right ventricle and lead to right ventricle dilation.
There a large variety of methods available in the prior art to treat different types of valvular heart disease such as pulmonic regurgitation and aortic regurgitation. A highly popular and successful method of treatment of these conditions involves the use of prosthetic cardiac valves, such as mechanical valves and bioprosthetic valves.
The most commonly used replacement devices are mechanical and bioprosthetic valves, with homografts and autografts less commonly used. From 1990 to 2000, the breakdown of valve replacement percentages as indicated by the Society of Thoracic Surgery Registry for patients less than 60 years of age with aortic valve disease was a follows: mechanical valves in 77% of patients, bioprosthetic valves in 13%, homograft valves in 5%, and the Ross procedure in 5%.
A mechanical valve is a device constructed from man-made materials and is used to replace patients damaged or diseased native heart valves. More than 60 percent of heart valve replacements have been made with mechanical prostheses due to their durability and superior hemodynamics which offer minimal resistance to flow. Despite their superior durability, the turbulent fluid mechanics of mechanical valves causes damage to blood cells. This damage to the blood cells can include thrombus formation. The possible thrombus formation initiated by disturbed flow patterns necessitates lifelong anticoagulant therapy. Further problems are associated with mechanical heart valves, including small stagnant regions proximate the hinges that sometimes lead to bacterial infections causing further heart damage.
Many different valve designs with different materials of construction have evolved to address the deficiencies of mechanical valves, such as to reduce thrombus formation and decrease the mechanical stresses that can cause blood cell damage. Several synthetic polymers have been tested as leaflet materials such as silicone, polyolefin rubbers and polytetrafluoroethylene. Laboratory fatigue testing has illustrated that polyurethane valves are capable of achieving more than 800 million cycles (˜20 years of “normal” function). Valve leaflets constructed of a commercially available polyetherurethane when implanted in sheep showed superior valve function to that of bioprosthetic valves. Thus, polymeric valves could offer a clinical advantage with the promise of improved durability compared to bioprostheses and low thrombogenicity compared to mechanical valves. Although polymeric valves show great promise they have been under development for several decades and no design has made it to commercialization due to failure or calcification within its normal biological environment. As a result, mechanical valves are still the primary choice for surgical correction and have to be used in conjunction with anticoagulation therapies, which reduces the quality of life of the patient and exposes them to risks associated with bleeding.
Bioprosthetic valves are tissue valves made of animal tissue (i.e. xenografts) and are easily and readily available. These were introduced in the early 1970s as an attempt to avoid some of the disadvantages of mechanical valves. Flexible, trileaflet, biological tissue valves mimic their natural counterparts more closely than mechanical heart valves. Their central flow characteristics offer better hemodynamic efficiency, and their biological surfaces enhance thromboresistance as compared to mechanical prostheses.
The valves are chemically treated to make the tissue less immunogenic and thus less likely to incite an allergic or immunological reaction in the recipient. As a result, the tissue comprising the valve is non-viable, and therefore, subject to degeneration with time. Bioprosthetic valves are commonly employed in elderly patients for whom the risk of bleeding complications are high and in those whose desired way of life precludes the discipline of anticoagulation therapy.
The biological tissues are usually fixed with different chemicals (glutaraldehyde, Aminooleic acid, ethanol etc) and under different protocols in order to increase the durability of the valve. Leaflet fixation stiffens the tissue unintentionally, alters internal shear properties, increases shear stiffness, stress relaxation and hysteresis, and causes substantial dehydration, all of which lead to valve failure due to calcification or tissue tearing. Although some chemical treatments are effective in reducing calcification, they do not prevent disruption of collagen fibers. Collagen fibers exposed to blood flow are damaged and cannot be repaired due to lack of viable cells within the leaflet. Therefore because of tissue degradation and calcification bioprosthetic valves have a limited durability which may average around 10 years. Although bioprosthetic valve technology has advanced, their limited durability is a problem which may take a long time to address completely.
Currently a new generation of bioprosthetic valves and mechanical valves is being developed, and these valves may be implanted percutaneously. While these bioprosthetic and mechanical valves present a number of improvements over the prior art, the safety and success of these devices is significantly reduced by the complexity of their deployment.
Many devices exist in the prior art, which attempt to address the complexity of properly deploying a bioprosthetic valve. For example, U.S. Pat. No. 6,790,230 to Beyersdorf et al. (“'230 patent”) discloses a conventional valve anchoring element, which has non-cylindrical form that corresponds to the shape of the aorta. The anchoring element of the '230 patent is provided such that a replacement valve can be sutured to the interior of the anchoring element. The anchoring element and associated replacement valve can then be delivered via a catheter to the aorta and expanded such as to disable the native aortic valve. Thereby, the expansion of the anchoring element in the aorta serves to disable the native aortic valve and, at the same time, enable the replacement valve.
U.S. Pat. No. 7,018,406 to Seguin et al. (“'406 patent) discloses a prosthetic valve assembly to be used in replacing a deficient native valve. The prosthesis described in the '406 patent includes a tissue valve supported on a self expandable stent. The prosthesis is capable of percutaneous delivery to the native valve, at which the prosthesis can be expanded and attached to the lumen wall. The '406 patent describes that the typical valve is made biological materials and is attached to the valve support band with a suture. The valve attached to the valve support band is collapsible along its center axis so that the entire structure can be compressed and loaded onto a catheter for delivery.
U.S. Patent Publication No. 2005/0137689 to Salahieh et al. (“'689 Publication”) discloses a method for endovascularly replacing a heart valve. The method disclosed in the '689 Publication includes the steps of delivering a replacement valve and an expandable anchor in an unexpanded configuration within a catheter to a vicinity of a heart valve. Once delivered to the proper location, the anchor is deployed from the catheter and expanded to contact tissue at an anchor site. The expansion of the anchor simultaneously deploys the collapsed replacement heart valve contained within the anchor.
The deployment of these conventional bioprosthetic valves requires the precise execution of a number of steps and techniques, and inaccurate execution of even one of these steps can lead to a patient fatality. For example, proper deployment of the bioprosthetic valve can require expansion of the valve anchor at a precise location within the native heart valve. Furthermore, the valve anchor must properly engage the lumen wall when expanded such that a good surface of contact is made with the lumen wall to enable a tight contact. Good and safe seating of the valve anchor is critical, as it must withstand blood flow under high pressure, high velocity, and a significant amount of pulsation. Furthermore, a replacement valve positioned in an inadequately anchored valve will not be able to resist the forces of the constantly changing vessel wall diameter and turbulent blood flow. Improper and insufficient deployment can lead to migration of the valve anchor before or after the deployment of the bioprosthetic valve. Even the slightest migration of the valve anchor can have many detrimental results, including covering the openings to an arterial outlet or compromising the function of the replacement valve.
Not only is precise placement of the valve anchor of a bioprosthetic valve important, a secure seating of the valve anchor is critical because improper or insufficient deployment of the valve anchor can lead to leakage between the anchor and the lumen wall. It is often the case that a deficient native valve and areas of tissue around the native valve have irregularities and calcification that are a result of, or are contributing factors to, the heart disease at issue. The typical calcification, thickening, and hardening of the cardiac annulus can make it increasingly difficult to achieve proper sealing quality for the valve anchor of the bioprosthetic valve. For example, heavy calcification on the native valve can lead to bumpy and even surfaces, which can translate to a low quality seal of the valve anchor with the lumen wall if not deployed properly. Not only can calcification make it difficult to properly seat the valve anchor, fragments of the calcified deposits can be loosened during the seating of the valve anchor and thus enter blood stream causing damage and possible blockage.
While many of the conventional devices have attempted to address the issues and complexities associated with the minimally invasive deployment of a heart valve replacement, significant problems and risks for the patient still exist. A large majority of the risk is due to the nature of the deployment of the replacement valves. Often, a surgeon has one shot to correctly deploy the heart valve prosthesis. Furthermore, the endovascular deployment of the heart valve provides a surgeon with a limited ability to verify the correctness and accuracy of the deployment. The surgeon's deployment of the replacement valve is often visually aided only by a two dimensional ultrasound image. This two dimensional image leaves a large amount of room for error in the three dimensional deployment of the replacement valve. For example, the valve anchor could appear properly seated on the ultrasound image, but the side of the valve anchor not visible in the image could be misaligned and/or improperly sealed with the lumen wall. As described, a slightly improper seal or slight misplacement of the valve anchor can lead to catastrophic and even fatal results. Additionally, once the replacement valve has been fully deployed, it is difficult or impossible to change the position of the prosthesis without damaging the native structure.
As a result of the limitations of both bioprosthetic heart valve and mechanical valves, patients have to choose between quality of life and durability of the repair. Additionally there is a group of patients which may not tolerate the risks associated with a mechanical valve, but may limit their lives using a bioprosthetic valve as a second operation to replace this valve can be considered clinically not viable.
Therefore, it would be advantageous to provide an apparatus and method to prepare a deficient native valve for replacement.
Additionally, it would be advantageous to provide an apparatus and method for accurate and efficacious deployment of a valve anchor.
Additionally, it would be advantageous to provide an apparatus and method for accurate and efficacious deployment of a valve anchor independent of a replacement heart valve.
Additionally, it would be advantageous to provide an apparatus and method for correcting valvular heart disease that allows for accurate and efficacious deployment of a heart valve prosthesis.
Additionally, it would be advantageous to provide an apparatus and method for correcting valvular heart disease that allows for viable methods to conduct repeat operations on a heart valve.
Additionally, it would be advantageous to provide an apparatus and method for correcting valvular heart disease that allows for viable methods to replace a previously deployed heart valve prosthesis.
Additionally, it would be advantageous to provide an apparatus and method for correcting valvular heart disease that allows for deployment of a replaceable heart valve prosthesis implemented in a minimally invasive manner.
Additionally, it would be advantageous to provide a releasably connected heart valve prosthesis delivered with a long arm or steerable needle from outside the heart to a valve of a beating heart.
Additionally, it would be advantageous to provide a smooth and substantially uniform surface within a lumen for deployment of a heart valve prosthesis.
Additionally, it would be advantageous to provide a backup system capable of permitting a patient to go on bypass if a heart valve replacement procedure fails.
Additionally, it would be advantageous to provide an apparatus capable of providing a separately deployable harbor for releasably connecting a heart valve prostheses.